Neurology Flashcards
1
Q
What condition is giant cell arteritis associated with?
A
Polymyalgia rheumatica
2
Q
Causes of cauda equina syndrome?
A
- herniated disc
- tumours (metastasis)
- spondylolisthesis (anterior displacement of a vertebra)
- abscess
- trauma
3
Q
What do the nerves of the cauda equina supply?
A
- sensation to the perineum, bladder and rectum
- motor innervation to lower limbs and anal & urethral sphincters
- parasympathetic innervation of the bladder and rectum
4
Q
Nerve roots of the cauda equina?
A
- L3-5
- S1-5
- coccygeal nerves
5
Q
Red flags for cauda equina syndrome?
A
- saddle anaesthesia (perineum)
- loss of sensation in bladder / rectum
- urinary retention / incontinence
- faecal incontinence
- bilateral sciatica
- bilateral / severe motor weakness in legs
- reduced anal tone
6
Q
Mechanism of action of neostigmine / pyridostigmine?
A
Blocks active site of acetylcholinesterase, increasing the amount of acetylcholine available to the post-synaptic membrane.
7
Q
What is alteplase?
A
Thrombolytic drug used to treat acute ischaemic stroke (also STEMI and PE).
8
Q
Mechanism of action of alteplase?
A
Converts plasminogen to plasmin, resulting in the lysis of fibrin.
9
Q
Recommended time window for alteplase after acute ischaemic stroke?
A
< 4.5 after symptom onset.
10
Q
What type of haemorrhage has a lucid interval?
A
Extradural haemorrhage
11
Q
Triggering factors for migraine?
A
- CHeese
- Oral contraceptive pill
- Caffeine
- alcohOL
- Anxiety
- Travel
- Exercise
- (chocolate)
12
Q
First line investigation for ischaemic stroke?
A
CT head
13
Q
Definition of ischaemic stroke?
A
Rapid onset of neurological impairment, lasting greater than 24 hours (or leading to death). Due to reduced / absent blood supply to an area of the brain leading to death of tissues.
14
Q
Initial treatment for ischaemic stroke?
A
300mg aspirin
15
Q
What is the pathophysiology of Parkinson’s disease?
A
- progressive neurodegeneration of dopaminergic neurones in the substantia nigra
- this leads to dopamine deficiency, resulting in impaired initiation of movements
- aggregation of alpha-synuclein forms Lewy bodies
16
Q
Signs of Parkinson’s?
A
- bradykinesia
- rigidity
- resting tremor
- postural instability
- shuffling gait
- expressionless face
17
Q
Eye movement disorder in Parkinson’s
A
Conjugate gaze disorder
18
Q
How is Parkinson’s investigated?
A
- PET scan with fluorodopa (shows decreased dopamine uptake in the substantia nigra)
- MRI brain
- DaTscan (type of SPECT to distinguish between Parkinson’s and essential tremor)
- serum ceruloplasmin / 24 hr urinary copper (exclude Wilson’s disease)
19
Q
What is SPECT?
A
single-photon emission computed tomography
20
Q
What is PET?
A
positron emission tomography
21
Q
Differentials for Parkinson’s?
A
- Wilson’s disease
- essential tremor
- drug-induced parkinsonism
22
Q
Pharmacological management of Parkinson’s?
A
- Levodopa (converted to dopamine)
- dopamine agonists
- MAO-B (monoamine oxidase) inhibitors
23
Q
Non-pharmacological management of Parkinson’s?
A
- deep brain stimulation
- physiotherapy
- speech and language therapy
24
Q
Complications of Parkinson’s?
A
- dementia
- depression
- sleep disorders
- falls
- dyskinesia due to medications
25
In what population of patients should sodium valproate not be used for seizures?
Females of child-bearing age, due to teratogenic effects.
26
First line treatment for new onset GTCS?
- lamotrigine
- topiramate
- oxcarbazepine
- levetiracetam
27
Side effects of long term levodopa use?
dyskinesia
28
Initial investigation for subarachnoid haemorrhage?
CT head
29
Investigation for SA haemorrhage if CT head is negative?
lumbar puncture
30
How is Guillain-Barre syndrome treated?
- IV immunoglobulin
| - plasmapheresis (plasma exchange)
31
What is the only disease-modifying drug for MND?
Riluzole (anti-glutamate medication).
32
Investigations for myasthenia gravis?
- serum anti-AChR antibodies / anti-MuSK antibodies
- repetitive nerve stimulation
- ice pack test (improves ptosis)
- CT / MRI chest - thymus gland assessment
33
How is the thymus involved in myasthenia gravis?
- 70% of patients have thymic follicular hyperplasia
| - 10% have thymoma
34
Initial presentation of myasthenia gravis vs LEMS?
- in myasthenia gravis, extra-ocular involvement is the most common initial presentation
- in LEMS, weakness of limbs is the most common initial presentation
35
Definition of transient ischaemic attack?
A transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia without acute infarction.
Sudden onset, lasts from a few minutes to 24 hours.
36
What is meant by crescendo TIA?
2 or more TIAs in a week - has a high risk of developing into stroke.
37
What causes TIA?
- thrombosis - due to atherosclerosis or small vessel disease (sickle cell anaemia, vasculitis)
- emboli - due to AF or carotid artery disease
- dissection (usually carotid) - may be spontaneous or secondary to trauma
38
Risk factors for TIA?
- smoking
- diabetes
- hypertension
- hypercholesterolaemia
- obesity
- AF
- carotid artery disease
- advancing age
- thrombophilic disorders (anti-phospholipid syndrome)
- sickle cell anaemia
- vasculitis
39
Pathophysiology of TIA?
Transient reduction in blood flow to an area of cerebral tissue, resulting in ischaemia causing focal neurological symptoms.
40
Clinical manifestations of TIA?
- unilateral muscle weakness
- unilateral sensory loss
- dysphasia
- ataxia / incoordination / vertigo
- amaurosis fugax
- homonymous hemianopia
- cranial nerve palsies
41
Investigations for TIA?
- clinical diagnosis
- head CT / MRI to rule out haemorrhage or infarction
- ABCD2 score to calculate stroke risk
- carotid dopplers (if patient is a candidate for carotid endarterectomy)
- lipid profile
- clotting profile (prothrombin time)
- ECG
42
What is the ABCD2 score?
Estimates risk of stroke following TIA.
43
Differentials for TIA?
- stroke
- hypoglycaemia
- seizure with Todd's paralysis
- complex migraine
- space-occupying lesion
44
Acute TIA management?
- assessment in specialist clinic on the day / next day
- calculate stroke risk (ABCD2 score)
- 300mg aspirin for 2 weeks
- DOAC for AF (instead of aspirin)
- consider carotid stenting / endarterectomy
45
What is carotid endarterectomy?
Surgery to remove plaque within carotid arteries?
46
When is carotid endarterectomy indicated?
If carotid artery is over 70% stenosed.
47
Long term prevention after TIA?
- 75mg clopidogrel (after two weeks of aspirin)
- anti-hypertensives
- statin therapy
- diabetic control
- lifestyle measures (physical activity, smoking cessation, diet optimisation, reduce alcohol)
- stop driving
48
Complications of TIA?
- stroke
| - MI
49
How many TIA patients go on to have a stroke?
Over 10% within 3 months.
50
What is amaurosis fugax?
Temporary painless blindness affecting one eye, as a result of ischaemia.
51
Aetiology of amaurosis fugax?
- obstruction of the ophthalmic artery / central retinal artery (branch of the ICA) due to atherosclerotic emboli
- optic neuritis
- giant cell arteritis
52
Risk factors for amaurosis fugax?
- TIA risk factors (smoking, hypertension, etc)
| - giant cell arteritis
53
Clinical manifestations of amaurosis fugax?
'Black curtain' comes across the vision.
54
Investigations for amaurosis fugax?
- eye examination
- carotid doppler ultrasound
- MR / CT angiography
55
Management of amaurosis fugax?
- control risk factors (statin therapy, anti-hypertensives. diabetes control)
- anticoagulation therapy (aspirin / clopidogrel)
- carotid stenting / endarterectomy
56
What is meant by stroke?
Cerebrovascular event caused by reduced / absent blood flow to cerebral tissue, resulting in tissue death. Characterised by sudden onset of focal neurological signs lasting longer than 24 hours.
57
What is the split between ischaemic and haemorrhagic stroke?
- ischaemic 85%
| - haemorrhagic 15%
58
Causes of haemorrhagic stroke?
- hypertension
- trauma
- anticoagulation
- tumour
- AV malformation
59
Most common cause of haemorrhagic stroke?
hypertension
60
Causes of ischaemic stroke?
- thrombosis (atherosclerosis or small vessel disease - vasculitis / sickle cell disease)
- emboli (AF or carotid artery disease)
- dissection (carotid), either spontaneous or secondary to trauma
61
How does carotid dissection result in ischaemic stroke?
Forms an intramural haematoma that compromises blood flow.
62
Risk factors for stroke?
- older age
- hypertension
- smoking
- diabetes
- hypercholesterolaemia
- obesity
- AF
- carotid artery disease
- thrombophilic disorders
- sickle cell disease
- vasculitis
63
Clinical manifestations of a stroke affecting the carotid territory?
- contralateral face / arm / leg weakness
- contralateral sensory loss
- dysphasia
- dysarthria
- homonymous hemianopia
- higher cortical dysfunction
64
Clinical manifestations of a stroke affecting the posterior circulation territory?
- ataxia
- dizziness
- dysarthria
- diplopia
- diplegia - paralysis affecting symmetrical parts of the body
- cranial nerve palsies
- visual field defects
- isolated homonymous hemianopia
- reduced GCS
65
Clinical manifestations of a lacunar stroke?
- motor hemiparesis
- ataxic hemiparesis
- 'clumsy hand'
- dysarthria
May be pure hemisensory, pure motor hemiparesis or mixed sensorimotor.
66
Clinical manifestations of a haemorrhagic stroke?
More likely to present with global features:
- focal neurological deficitis
- headache
- altered mental status
- nausea and vomiting
- seizures
67
Investigations for stroke?
- CT head (sensitive for haemorrhage, usually cannot diagnose acute phase infarct)
- MRI brain
- perfusion imaging (CT angiography) to check viable tissue and avoid reperfusion injury
68
Differentials for stroke?
- TIA
- seizure with Todd's paresis
- tumour / abscess
- migraine
- hypoglycaemia
69
Acute management of ischaemic stroke?
- aspirin 300mg (for 2 weeks)
- admit to specialist stroke unit
- IV alteplase for thrombolysis (within 4.5 hours)
- thrombectomy (within 6 hours)
70
What is the mechanism of action of alteplase?
Tissue plasminogen activator - produces plasmin that lyses fibrin.
71
Contraindications to alteplase?
- major recent surgery
- bleeding
- severe hypertension
- brain malignancies
72
Long term management of ischaemic stroke?
- lifestyle changes & stop driving
- occupational therapy & rehabilitation
- clopidogrel 75mg lifelong (after 2 weeks aspirin)
- DOAC for AF
- antihypertensives & statin therapy
73
Management of haemorrhagic stroke?
- ABCDE, monitor pupil responses and GCS
- correct coagulopathy / reverse anticoagulation
- BP control (acutely aim for < 140-160 systolic)
- neurosurgery
74
Early complications of stroke?
- seizures
- cerebral oedema
- death
75
Late complications of stroke?
- motor and sensory deficits
- bladder and bowel dysfunction
- cognitive problems
- visual problems
- psychological problems
- swallowing difficulties
76
What is a subarachnoid haemorrhage?
Sudden severe headache ('thunderclap headache') due to bleeding into the subarachnoid space.
77
Causes of SA haemorrhage?
- trauma
- aneurysm rupture
- AV malformation
78
Risk factors for SA haemorrhage?
- age > 50
- female
- smoking
- hypertension
- connective tissue disorders (Marfan's / EDS)
- family history
- polycystic kidney disease
79
Clinical manifestations of SA haemorrhage?
- severe sudden onset 'thunderclap' headache
- impaired / loss of consciousness
- meningismus (neck stiffness, muscle aches)
- photophobia
- nausea and vomiting
- Kernig's and Brudzinski's signs
80
Investigations for SA haemorrhage?
- CT head shows hyperdense areas in SA space
| - lumbar puncture if CT is negative, shows bloody CSF (performed at least 12 hrs after symptom onset)
81
Management of SA haemorrhage?
- supportive care: intubation and sedation may be required, O2, analgesia
- nimodipine (CCB to prevent delayed cerebral ischaemia)
- neurosurgery (endovascular coiling, surgical clipping)
82
Complications of SA haemorrhage?
- obstructive hydrocephalus
- arterial vasospasm
- re-bleeding of aneurysm
- long-term neurological deficits
83
What causes delayed cerebral ischaemia in SA haemorrhage?
Arterial vasospam
84
Mortality from SA haemorrhage?
50%
85
What is a subdural haemorrhage?
Collection of blood between the dura mater and arachnoid mater.
86
Over what time frame may a subdural haemorrhage occur?
- acute (< 3 days)
- subacute (3-21 days)
- chronic (21 days)
87
Causes of subdural haemorrhage?
- trauma (temporal side of head, causes rupture of bridging veins)
- cerebral aneurysm rupture
- AV malformation rupture
88
Risk factors for subdural haemorrhage?
- history of trauma / loss of consciousness
- vulnerability to falls (dementia)
- age > 65
- anticoagulation / coagulopathy
- alcohol misuse
89
Pathophysiology of subdural haemorrhage?
- haematoma volume increases, causing compression and displacement of the brain parenchyma
- ICP rises, which may lead to brain herniation
90
Clinical manifestations of subdural haemorrhage?
Gradual deterioration:
- headache
- nausea and vomiting
- impaired consciousness / confusion
- ataxia / poor balance
- cranial nerve palsies
- seizures
91
Investigations for subdural haemorrhage?
- non-contrast CT head (shows crescent shaped collection of blood)
- MRI brain to identify an underlying cause
- coagulation screen
92
Acute vs chronic subdural haemorrhage appearance on CT?
Acute - hyperdense (white).
| Chronic - hypodense.
93
Management of subdural haemorrhage?
- correct coagulopathy / anticoagulation reversal
- anticonvulsants
- conservative management for small bleeds
- decompressive craniectomy
- burr hole craniotomy for chronic subdural haemorrhage
94
Complications of subdural haemorrhage?
- permanent neurological deficits
- coma
- seizures
- intracranial infection
- recurrent subdural haematoma
95
What is an extradural haemorrhage?
Acute haemorrhage between the dura mater and the inner surface of the skull.
96
Causes of extradural haemorrhage?
Skull trauma in the temporoparietal region (often involves middle meningeal artery) - falls, assault, sporting injuries.
Other causes such as AV malformations and bleeding disorders.
97
Pathophysiology of extradural haemorrhage?
- as the haematoma grows in volume, it strips the dura mater away from the skull
- ICP increases, leading to midline shift and tentorial herniation, and eventually brainstem death
98
Clinical manifestations of extradural haemorrhage?
Immediate loss of consciousness, lucid period, then progressive decrease in consciousness.
- headache
- nausea and vomiting
- confusion
- motor / sensory limb defects
- cushing's triad
99
Investigations for extradural haemorrhage?
- CT head shows lemon shaped haemorrhage with midline shift
| - blood glucose (exclude hypoglycaemia)
100
Management of extradural haemorrhage?
- correct coagulopathy / anticoagulation reversal
- prophylactic antibiotics
- anticonvulsants
- mannitol / barbiturates to reduce ICP
- burr hole craniotomy
- decompressive hemicraniectomy for large bleeds
101
Complications of extradural haemorrhage?
- infection
- cerebral ischaemia
- seizures
- hydrocephalus
- brainstem injury
102
What is the definition of epilepsy?
Condition characterised by recurrent seizures unprovoked by any immediate identified cause.
2 or more unprovoked seizures separated by at least 24 hours.
103
What is the definition of an epileptic seizure?
Paroxysmal event in which changes of behaviour, sensation, or cognitive processes are caused by excessive, hyper-synchronous neuronal excitation in the brain.
104
Pathophysiology of epileptic seizures?
Abnormal properties of neurons lead to inappropriate hyperexcitability and hypersynchrony.
105
Initiation of generalised-onset seizures?
Bihemispheric electrical discharges.
106
Initiation of focal-onset generalised seizures?
Initially a focal seizure occurs, then the electrical discharges evolve through the ipsilateral hemisphere and cross the corpus callosum to continue in the contralateral hemisphere.
107
Clinical manifestations of GTCS?
- loss of consciousness
- tonic phase (muscle tensing) followed by clonic phase (muscle jerking)
- tongue biting
- incontinence
- irregular breathing
- post-ictal period where patient is confused, drowsy and irritable / depressed
108
Investigations for GTCS?
- video EEG (shows generalised epileptiform activity)
- head CT / MRI may show a structural lesion
- lumbar puncture (elevated WCC in CNS infection)
109
Differentials for GTCS?
- syncope
- cardiac arrhythmia
- transient ischaemic attack
110
Pharmacological management of GTCS?
Monotherapy with an anticonvulsant - try two different drugs before initiating dual therapy.
- carbamazepine
- lamotrigine
- topiramate
- sodium valproate
111
Summary of management of GTCS?
- anti-convulsant medication
- surgical resection (in patients with drug-resistant focal onset epilepsy)
- deep brain / vagus nerve stimulation
112
What are focal seizures?
Seizures arise in one portion of the brain, commonly the temporal lobe. They may affect hearing, speech, memory and emotions.
113
Pathophysiology of focal seizures?
Hyperexcitability and hypersynchronicity of a group of neurons in one area of the brain.
114
Clinical manifestations of focal seizures?
- movement of a specific body part
- sense of premonition (fear, deja vu)
- automatisms (lip smacking, clothes picking)
- staring and being unaware of surroundings
- visual, olfactory or gustatory hallucinations
115
Investigations for focal seizures?
- video EEG
- head CT / MRI for structural abnormalities
- lumbar puncture and CSF fluid analysis for signs of infection
116
Differentials for focal seizures?
- syncope
- TIA
- tic disorders
- tremor
- dissociative disorders
- migraine
117
Management of acute focal seizures?
Benzodiazepines (rectal diazepam, intranasal midazolam, oral lorazepam, IV benzodiazepines in hospital).
118
Long-term anticonvulsant therapy for focal seizures?
Monotherapy of two different drugs, then trial dual therapy:
- lamotrigine
- levetiracetam
- oxcarbazepine
119
Which anticonvulsants should be avoided in women of child-bearing age?
- sodium valproate
- topiramate
- phenobarbital
- phenytoin
Enzyme-inducing anticonvulsants lower efficacy of the oral combined contraceptive pill (e.g. carbamazepine).
120
Options for treatment-resistant epilepsy?
- surgical resection of localised epileptogenic area
| - neurostimulation (vagus nerve / deep brain stimulation)
121
What is meant by status epilepticus?
Convulsive seizure lasting > 5 minutes, or repetitive convulsive seizures with no recovery in between.
122
Causes of status epilepticus?
- anticonvulsant drug withdrawal
| - poor anticonvulsant therapy adherence
123
Pathophysiology of status epilepticus?
- mechanisms that normally abort seizure activity fail, there is excessive and abnormally persistent neuronal excitation
- neuronal injury occurs due to the accumulation of excitatory neurotransmitters
124
How is status epilepticus managed?
- ABCDE (secure airway, semi-prone position)
- supportive care and monitoring
- IV benzodiazepine (lorazepam)
125
What is Parkinson's disease?
Chronic, progressive neurodegenerative condition that occurs secondary to loss of dopaminergic neurones within the substantia nigra.
126
What is meant by Parkinsonism?
Refers to the presence of bradykinesia and resting tremor / rigidity / postural instability.
127
Risk factors for Parkinson's disease?
- male
- older age
- family history
- head trauma
128
What is meant by 'on-off' fluctuations?
Patients switch from dyskinesia to immobility in a few minutes.
129
What is essential tremor?
Progressive, symmetrical movement disorder of the hands and forearms. Absent at rest, present during intentional movements (particularly anti-gravity positions).
130
Investigations for essential tremor?
- MRI brain
| - DaTscan to distinguish between Parkinson's and essential tremor
131
What is Huntington's disease?
Autosomal dominant neurodegenerative condition - characterised by chorea, dystonia, and cognitive changes.
132
Cause of Huntington's disease?
Abnormal expansion of the CAG trinucleotide in the huntingtin gene on chromosome 4.
133
What is meant by anticipation in Huntington's disease?
More severe disease develops at an earlier age in offspring.
134
Pathophysiology of Huntington's disease?
- CAG expansion leads to an elongated polyglutamine tail on the huntingtin protein
- cleavage and aggregation of this abnormal protein causes neuronal damage
- loss of neurons results in GABA and ACh depletion, dopamine is spared
- primarily affects the striatum (caudate and lentiform nuclei)
135
What does the lentiform nucleus consist of?
- caudate nucleus
| - globus pallidus
136
Clinical manifestations of Huntington's?
Development of psychiatric features and cognitive decline, followed by motor features.
137
Psychiatric features of Huntington's?
- depression
- paranoia / delusions
- irritability
- impulsivity
- disinhibition
- obsessions and compulsions
- personality change
138
Cognitive features of Huntington's?
- impaired work performance
- impaired concentration
- memory loss and dementia
- difficulties with multi-tasking and complex decisions
139
Motor features of Huntington's?
- chorea (abrupt, abnormal, involuntary movements)
- loss of co-ordination
- dysphagia and dysarthria
- dystonia (involuntary muscle contraction causing repetitive or twisting movements)
- eye movement disorders
140
Investigations for Huntington's?
Genetic testing - PCR analysis and gel electrophoresis.
141
Summary of Huntington's disease management?
- pharmacological therapies
- physiotherapy and occupational therapy
- speech and language therapy
- neuropsychiatric management
- palliative care
- genetic counselling
142
Pharmacological therapies for Huntington's?
- dopamine depleting agents
| - treatment of chorea with anti-psychotics / benzodiazepines
143
Neuropsychiatric management in Huntington's?
- SSRIs for depression
- anti-psychotics (e.g. risperidone)
- CBT
144
Life expectancy in Huntington's?
15-20 years from symptoms onset.
145
Common causes of death in Huntington's?
- respiratory disease (e.g. pneumonia)
| - suicide
146
What is the definition of dementia?
Syndrome characterised by a significant deterioration in mental function, leading to impairment of normal function and ability to carry out ADLs.
147
What is the most common cause of dementia?
Alzheimer's (50-75% of cases)
148
Risk factors for Alzheimer's?
- older age
- CVD risk factors
- depression
- head trauma
- low social engagement and support
- Down's syndrome
- cerebrovascular disease
149
Why is Down's syndrome associated with AD?
Amyloid precursor protein (APP) gene is found of chromosome 21.
150
Pathophysiology of AD?
- formation of senile plaques and neurofibrillary tangles in the hippocampus and medial temporal lobes
- senile plaques are extracellular deposits of aggregated beta-amyloid, formed from the breakdown of APP
- neurofibrillary tangles are intracellular aggregations of hyperphosphorylated tau protein, which promote neuronal death
151
Clinical presentation of AD?
Memory impairment is the initial presentation - short term memory loss and difficulty learning new information.
152
Signs and symptoms of AD?
- memory loss
- disorientation
- nominal dysphasia
- apathy
- personality and mood changes
- psychiatric problems
- disinhibition
- loss of higher cognitive function (multitasking and complex tasks)
153
Cognitive testing in AD?
Mini mental state examination (score out of 30). 0-17 is considered severe cognitive impairment.
154
Investigations for AD?
- MMSE / neuropsychological testing
- head CT / MRI
- fluorodeoxyglucose-PET to localise areas of brain involvement
- lumbar puncture and CSF analysis (may show amyloid / tau biomarkers)
155
Which areas of the brain are affected by AD?
Hippocampus and medial temporal lobes.
156
Pharmacological therapy for AD?
- acetylcholinesterase inhibitors (donepezil, rivastigmine)
| - memantine for severe AD
157
What is frontotemporal dementia?
Neurodegenerative disorder characterised by focal degeneration of the frontal and temporal lobes. Causes disturbances in behaviour, personality and language.
158
Epidemiology of frontotemporal dementia?
- common cause of early onset dementia (< 65 years)
| - accounts for 2% of dementia cases
159
Cause of frontotemporal dementia?
Strong genetic predisposition.
160
Which variant of FTD is more common?
Behavioural
161
Pathophysiology of FTD?
- neuronal loss results in frontal / temporal lobe degeneration
- abnormal protein inclusions may be seen in neurons and glial cells (hyperphosphorylated tau)
162
Clinical manifestations of the behavioural variant of FTD?
- disinhibition
- loss of empathy
- apathy
- compulsive behaviour
163
Clinical manifestations of primary progressive aphasia?
- effortful speech
- halting speech
- articulation difficulties
- word-finding difficulty
164
What are the subtypes of FTD?
- behavioural variant
| - primary progressive aphasia
165
Investigations for FTD?
- cognitive assessment (MMSE)
| - MRI brain
166
Management of FTD?
- SSRIs for difficult behavioural symptoms
- occupational therapy
- physiotherapy
- speech and language therapy
167
What is Lewy body dementia?
Rapidly progressive dementia characterised by Lewy body (alpha-synuclein) deposition in the brain.
168
Clinical manifestations of Lewy body dementia?
- cognitive impairment (difficulties multitasking and performing complex tasks)
- visual hallucinations
- Parkinson-like symptoms
169
What is vascular dementia?
Common form of dementia caused by cerebrovascular disease.
170
What is mixed dementia?
Combination of Alzheimer's and vascular dementia.
171
How many cases of dementia are vascular?
20%
172
Causes of vascular dementia?
- ischaemic stroke
- multiple small cerebrovascular infarcts
- small vessel disease (atherosclerosis)
- haemorrhage
- amyloid deposition in small arteries
173
Risk factors for vascular dementia?
- age > 60
- hypertension
- smoking
- hypercholesterolaemia
- diabetes
174
Clinical presentation of vascular dementia?
Stepwise cognitive decline.
175
Signs and symptoms of vascular dementia?
- poor memory
- dysphasia
- impaired higher cognitive function (planning and problem-solving)
- disorientation
- agitation
- depression and anxiety
- disinhibition
- disturbed sleep cycle
- apathy
- focal neurological signs (due to previous stroke)
176
Investigations for vascular dementia?
- cognitive assessment tool (MMSE)
| - MRI head
177
Management of vascular dementia?
- control CVD risk factors
- pharmacological therapies (most useful in patients with mixed dementia)
- group cognitive stimulation programmes
- physical activity
178
What is the definition of migraine?
Chronic, episodic neurological disorder that causes headache and other associated symptoms. May occur with or without aura.
179
What might trigger a migraine?
- stress
- bright lights
- strong smells
- certain foods
- dehydration
- menstruation
- disturbed sleep patterns
180
Pathophysiology of migraine?
- neurogenic inflammation of first-division (ophthalmic) trigeminal sensory neurons that innervate the meninges and large vessels of the brain
- activated trigeminal neurons release substances causing sensitisation of peripheral nociceptors and subsequently central sensitisation
181
What causes aura in migraine?
Neuronal dysfunction results in waves of neuronal excitation spread anteriorly in the cortex.
182
Signs and symptoms of migraine?
- prolonged headache of moderate / severe intensity
- nausea and vomiting
- sound sensitivity and photosensitivity
- aura
- throbbing sensation
183
Is migraine unilateral or bilateral?
Most commonly unilateral, but over 40% are bilateral.
184
What are some examples of aura?
- visual sparkles, flashing lights
- visual loss or blind spots
- numbness / tingling of the face or hands
- dysphasia may occur
185
What is a hemiplegic migraine?
Stroke mimic:
- hemiplegia
- ataxia
- changes in consciousness
186
Investigations for migraine?
To exclude differentials:
- lumbar puncture and CSF analysis
- CT / MRI head
187
Management of migraines?
1. NSAID + anti-emetic + hydration
2. paracetamol + anti-emetic + hydration
3. paracetamol/aspirin/caffeine + anti-emetic + hydration
Severe symptoms - triptans (serotonin receptor agonists).
Lifestyle measures - regular meals, sleep hygiene, avoid triggers, etc.
188
What is 5-HT?
Serotonin
189
How do triptans work in migraines?
- cause vasoconstriction of arteries by acting on smooth muscle
- inhibit the activation of peripheral pain receptors
- reduce neuronal activity
190
What are tension headaches?
Episodic or chronic headaches, pain is like a tight band around the head.
191
Causes of tension headaches?
- stress
| - disturbed sleep patterns
192
What are cluster headaches?
Unilateral headaches lasting 15-180 minutes, associated with autonomic symptoms.
Considered one of the most painful conditions known.
193
Pathophysiology of cluster headaches?
- trigeminal nerve carries nociceptive information from pain-sensitive structures in the face to the brainstem
- from the brainstem, information is sent to the cortex via pain-processing pathways after synapsing in the trigeminocervical complex
- afferent trigeminal signals arriving at the trigeminocervical complex activates the cranial parasympathetic nervous system
194
Signs and symptoms of cluster headaches?
- repeated attacks of excruciating unilateral pain lasting 15-180 minutes
- nausea and vomiting
- photophobia / phonophobia
- aura
- autonomic features (lacrimation, rhinorrhoea, etc)
195
Acute management of cluster headaches?
- subcutaneous sumatriptan
| - oxygen therapy
196
Long-term management of cluster headaches?
- corticosteroid transitional therapy
- preventative therapy: verapamil
- deep brain stimulation
197
What is idiopathic intracranial hypertension?
Disorder caused by chronically elevated ICP - leading to headache, papilloedema, and vision loss.
198
Typical idiopathic intracranial hypertension patient?
Female, obese, child-bearing age.
199
Signs and symptoms of IIH?
- headache (worse lying down or bending over)
- transient vision loss
- vision loss
- photopsia (flashes of light)
- tinnitus
- papilloedema
- diplopia (due to CN VI palsy)
200
Investigations for IIH?
- lumbar puncture (high opening pressure)
- fundoscopy
- MRI brain
201
Signs of papilloedema on fundoscopy?
- venous engorgement
- loss of venous pulsation
- haemorrhages adjacent to optic disc
- blurring of optic margins
202
Management of IIH?
- weight loss (with low sodium diet)
- serial lumbar punctures
- carbonic anhydrase inhibitor (to reduce production of CSF)
- furosemide
- neurosurgical interventions
203
What is giant cell arteritis?
Systemic granulomatous vasculitis primarily affecting branches of the external carotid artery. Symptoms typically affect the temporal artery.
204
What disease is associated with giant cell arteritis?
Polymyalgia rheumatica
205
What is polymyalgia rheumatica?
Inflammatory disorder causing pain and stiffness in the muscles around the shoulders, neck, and hips.
206
Pathophysiology of GCA?
- immune insult occurs in the outer (adventitial) layer of the arterial wall
- dendritic cells attract T cells and present antigens to them
- T helper cells enter the artery via the vasa vasorum, become activated and undergo clonal expansion in the artery wall
- T cells release interferon gamma which stimulates macrophages and induces multinucleated giant cell formation
- macrophages release cytokines, causing damage to the arterial wall
- the artery releases growth and angiogenic factors, leading to intimal expansion and hyperplasia
- this results in narrowing and occlusion of the vessel lumen, causing ischaemia
207
Histological appearance of GCA?
Arteries contain inflammatory skip lesions composed of T cells and macrophages. Multinucleated giant cells are present in around 50% of cases.
208
Signs and symptoms of GCA?
- severe unilateral headache around the temple
- amaurosis fugax / blurred vision / vision loss
- arterial thickening / nodularity
- scalp tenderness
- jaw claudication
- muscle aches and stiffness in shoulders, neck and hips
209
Gold standard investigation for GCA?
Temporal artery biopsy.
210
Investigations for GCA?
- temporal artery biopsy
- CRP / ESR
- vascular ultrasound - wall thickening ('halo' sign), stenosis, occlusion
211
Management of GCA?
- high dose corticosteroids (reduce risk of site loss)
- aspirin 75mg daily
- bone and gastric protection (bisphosphonates, PPI)
212
Complications of GCA?
- stroke
| - vision loss
213
What is trigeminal neuralgia?
Facial pain syndrome in the distribution of one or more divisions of the trigeminal nerve. Characterised by paroxysms of sharp, stabbing pain, or a constant component of facial pain.
214
Causes of trigeminal neuralgia?
Classical - vascular compression of the trigeminal root by tortuous or aberrant vessels.
Symptomatic - caused by a structural lesion such as a tumour or MS.
215
Pathophysiology of trigeminal neuralgia?
Neuropathic pain is caused by focal demyelination of trigeminal neurons, resulting in conduction abnormalities.
216
Management of trigeminal neuralgia?
- anticonvulsant (carbamazepine)
| - microvascular decompression surgery
217
What is cauda equina syndrome?
Compression of the collection of nerves distal to the terminal part of the spinal cord. Syndrome characterised by lower limb weakness, bladder and bowel dysfunction, and abnormal perianal sensation.
218
What vertebral level does the cauda equina start?
L2
219
What nerve roots does the cauda equina contain?
L2 - Co1
220
Causes of cauda equina syndrome?
- lumbar stenosis (narrowing of the spinal canal)
- spinal trauma
- disc herniation
- malignancy
- spinal infections (e.g. abscess)
- neural tube defects
221
Is cauda equina syndrome an UMN lesion or a LMN lesion?
LMN lesion
222
Signs and symptoms of cauda equina syndrome?
- lower back pain
- asymmetrical sciatica pain (alternating buttock pain)
- saddle anaesthesia
- bladder dysfunction (urinary retention / overflow incontinence)
- bowel dysfunction (constipation, incontinence, loss of anal tone)
- asymmetrical lower limb weakness / sensory changes
- hypotonia and hyporeflexia
223
Gold standard investigation for cauda equina syndrome?
MRI spine
224
Management of cauda equina syndrome?
Neurosurgical emergency requiring decompressive surgery.
225
Complications of cauda equina syndrome?
- bladder and bowel dysfunction
- sexual dysfunction
- chronic pain
- paralysis
226
What is multiple sclerosis?
Chronic, progressive condition involving demyelination of neurons in the CNS. Caused by autoimmune activation against myelin and subsequent inflammation.
227
Definition of MS?
The presence of episodic neurological dysfunction in at least two areas of the CNS, separated in space and time.
228
What is progressive-relapsing MS?
Progressive worsening of the condition from the beginning, with distinct attacks of symptoms occurring throughout the course of the disease.
229
What is secondary progressive multiple sclerosis?
Initially follows a relapsing-remitting course, then there is progressive worsening.
230
What is primary progressive MS?
Progressive worsening of the condition from the beginning, without distinct attacks of symptoms.
231
What is relapsing-remitting MS?
Distinct attacks of symptoms partially resolve, leaving residual disability. Subsequent attacks cause an increase in disability. There is no progression of the condition between the attacks.
232
Cause of MS?
Autoimmune disease - combination of genetic factors and environmental triggers.
233
Typical MS patient?
Female, aged 20-40.
234
What type of hypersensitivity reaction is involved in MS?
Type IV - cell-mediated.
235
Pathophysiology of MS?
- T cell crosses the BBB and becomes activated by myelin
- activated T cell causes upregulation of endothelial adhesion molecules, allowing passage of more immune cells across the BBB
- T cell releases cytokines, attracting B cells and macrophages
- B cells produce antibodies against myelin
- macrophages phagocytoses oligodendrocytes
- destruction of oligodendrocytes causes demyelination of axons, leaving areas of scar tissue (plaques)
236
Pathophysiology of relapsing-remitting MS?
- regulatory T cells act to inhibit the immune response and reduce inflammation
- this allows remyelination to occur in early MS
- eventually irreversible damage and permanent demyelination occur
237
What are some clinical manifestations of MS?
- optic neuritis
- eye movement abnormalities
- focal weakness (Bell's palsy, Horner syndrome, limb paralysis, incontinence)
- focal sensory symptoms (trigeminal neuralgia, numbness / paraesthesia)
- ataxia
238
What is the most common presentation of MS?
Optic neuritis
239
What are some features of optic neuritis?
- central scotoma (blind spot)
- pain on eye movement
- impaired colour vision
240
What is Horner syndrome?
Unilateral:
- ptosis
- miosis (constricted pupil)
- anhidrosis (absence of sweating)
241
Investigations for MS?
- MRI brain
- lumbar puncture with CSF electrophoresis (shows oligoclonal IgG bands)
- visual evoked potential - measures speed of nerve impulses along the optic nerve in response to visual stimuli
242
Differentials for MS?
- ischaemic stroke
- Guillian-Barre syndrome
- vitamin B12 deficiency
- fibromyalgia
243
What are some disease-modifying drugs for MS?
- recombinant interferon beta (interferes with demyelinating plaque formation)
- immunosuppressants
244
Treatment for MS relapse?
Methylprednisolone
245
Treatment for spasticity in MS?
- baclofen
- gabapentin
- physiotherapy
246
What is myasthenia gravis?
Chronic autoimmune disorder of the post-synaptic membrane at the neuromuscular junction in skeletal muscle. Characterised by muscle weakness and fatiguability.
247
What is the bimodal peak in incidence for myasthenia gravis?
- females aged 20-30
| - males aged 60-70
248
What type of hypersensitivity reaction is involved in myasthenia gravis?
Type II (antibody mediated).
249
Pathophysiology of myasthenia gravis?
- anti AChR antibodies bind to ACh-R on the motor end plate of skeletal muscle, blocking the binding of ACh
- there is a reduction in the number of ACh receptors on the post-synaptic membrane
- complement-mediated destruction of the post-synaptic membrane reduces the surface area available for new ACh-R insertion
250
What are some ocular manifestations of myasthenia gravis?
- diplopia
| - ptosis
251
What are some respiratory manifestations of myasthenia gravis?
- breathlessness
- weak breathing
- respiratory failure
252
What are some bulbar manifestations of myasthenia gravis?
- fatiguable chewing
- dysarthria
- dysphagia
253
What are some limb manifestations of myasthenia gravis?
- dropped head
- proximal affected more than distal
- arms affected more than legs
254
What is the ice pack test?
Improvement in ptosis after the application of an ice pack to the closed eyelids for 2 minutes.
255
What is myasthenic crisis?
Worsening of muscle weakness requiring respiratory support.
256
Investigations for myasthenic crisis?
- serum anti-AChR antibodies / anti-MuSK antibodies
- repetitive nerve stimulation / electromyography
- ice pack test
- CT / MRI chest (to assess thymus gland)
257
Management of myasthenia gravis?
- acetylcholinesterase inhibitor (pyridostigmine)
- corticosteroids (prednisolone)
- immunosuppressants (azathioprine)
- thymectomy - if patients have thymoma
258
Side effects of pyridostigmine?
- diarrhoea
- urinary incontinence
- GI upset
- bronchospasm
- sweating
259
How is myasthenic crisis managed?
- HDU / ITU admission
- respiratory support if needed (intubation and ventilation)
- IVIG and plasma exchange
- prednisolone
260
What is Lambert Eaton myasthenic syndrome?
Autoimmune disorder of the neuromuscular junction. Characterised by the presence of circulating antibodies against voltage-gated calcium channels.
261
What causes LEMS?
- paraneoplastic syndrome (e.g. associated with small cell lung cancer)
- non-paraneoplastic LEMS occurs due to a general autoimmune state
262
Pathophysiology of LEMS?
- antibodies are produced against voltage-gated calcium channels
- anti-VGCC antibodies damage the calcium channels in the presynaptic terminals of the neuromuscular junction
- this inhibits the release of ACh into the synaptic cleft, inhibiting muscle contraction
263
Signs and symptoms of LEMS?
- limb weakness (proximal)
- dysarthria
- ptosis and diplopia
- dysphagia
- autonomic symptoms: dry mouth, orthostatic hypotension, erectile dysfunction
264
Investigations for LEMS?
- repetitive nerve stimulation / electromyography
- serum anti-VGCC antibodies
- imaging tests for small cell lung cancer (CT, MRI, PET)
265
Management of LEMS?
- manage underlying malignancy
- amifampridine - allows release of more ACh into the synaptic cleft
- immunosuppressants (prednisolone / azathioprine)
- IVIG
- plasma exchange
266
Mechanism of action of amifampridine?
Blocks voltage-gated potassium channels in the pre-synaptic terminal, prolonging the depolarisation of the cell membrane to allow the release of more ACh into the synaptic cleft.
267
What is Guillain-Barré syndrome?
Acute inflammatory polyneuropathy - characterised by a progressive, symmetrical, ascending neuropathy resulting in weakness and reduced reflexes. The majority of patients have a history of preceding illness.
268
Infective causes of GBS?
- campylobacter jejuni
- cytomegalovirus
- Epstein-Barr virus
269
What is the pathophysiology of GBS?
- immune-mediated damage to peripheral nerves
- ‘molecular mimicry’ occurs, where antibodies generated in response to pathogens cross-react with the body’s nerve cells
- antibodies target the myelin sheath
270
Clinical manifestations of GBS?
- progressive symmetrical weakness in limbs, ascending from distal muscles
- respiratory muscle involvement
- reduced tendon reflexes
- reduced sensation / paraesthesia
271
What is Miller Fisher syndrome?
GBS variant characterised by:
- ataxia
- areflexia
- ophthalmoplegia
272
What is ophthalmoplegia?
Paralysis of extraocular muscles due to involvement of CN III, IV or, VI.
Diplopia is a characteristic symptom.
273
Investigations for GBS?
- lumbar puncture
- antibody screen (anti-GQ1b is specific for Miller Fisher syndrome)
- spirometry to monitor respiratory function
- nerve conduction studies / electromyography
274
What is electromyography?
Measures electrical activity in response to a nerve’s stimulation of muscle. Involves the insertion of electrodes (needles) through the skin into the muscle.
275
Gold standard for GBS diagnosis?
Lumbar puncture - high CSF protein with normal CSF WCC.
276
Management of GBS?
- IVIG
- plasma exchange
- ventilation
277
Complication of GBS?
Respiratory failure.
278
Contraindications for lumbar puncture?
- raised ICP
- decreased GCS
- coagulopathy
- infection at the site of lumbar puncture
279
What is carpal tunnel syndrome?
Entrapment of the median nerve against the carpal tunnel.
280
Risk factors for carpal tunnel syndrome?
- diabetes
- osteoarthritis
- obesity
- hypothyroidism
- pregnancy
- trauma
281
Pathophysiology of carpal tunnel syndrome?
- anatomical compression of the median nerve occurs due to flexor tendon fibrosis, a mass lesion, or an anatomically small tunnel
- inflammation of the median nerve occurs in response to the compressive injury
282
Sensory innervation provided by the median nerve?
Palmar and distal dorsal aspects of the lateral three-and-a-half digits.
283
Motor innervation provided by the median nerve?
2LLOAF
284
Nerve roots of the median nerve?
C6, C7, C8, T1
285
Signs and symptoms of carpal tunnel syndrome?
- dull ache / discomfort in wrist, fingers, or forearm
- paraesthesia
- weakness
- clumsiness & difficulty opening jars, buttoning shirts, etc.
- sensory loss
- thenar eminence wasting
- weak thumb abduction and opposition
286
Management of carpal tunnel syndrome?
- wrist splints
- physiotherapy
- corticosteroids
- open / laparoscopic carpal tunnel release
287
Features of UMN lesion?
- hypertonia
- hyperreflexia
- spasticity
- Babinski reflex
- ankle clonus
- jaw clenching
288
Features of LMN lesion?
- hypotonia
- hyporeflexia
- fasciculations
- muscle cramps
- muscle atrophy
- weakness
289
Key mutations in familial MND?
- C9orf72
| - SOD-1
290
Pathophysiology of MND?
- progressive degeneration of both upper and lower motor neurons
- sensory neurons are spared
291
Pharmacological therapy for MND?
- riluzole (anti-glutamate medication)
- baclofen for muscle cramps
- opioid therapy for breathlessness
292
What is Bell’s palsy?
Unilateral facial nerve palsy of known cause.
293
What is the most common cause of facial palsy?
Bell’s palsy
294
Presentation of Bell’s palsy?
Rapid onset (< 72 hours) of unilateral facial weakness.
295
Signs and symptoms of Bell’s palsy?
- unilateral facial weakness
- post-auricular / ear pain
- difficulty chewing
- drooling
- incomplete eye closure
- hyperacusis
- loss of nasolabial fold (smile lines)
- no forehead sparing
- eyebrow drooping
- asymmetrical smile
296
Why is there no forehead sparing in Bell’s palsy?
LMN lesion
297
What is Bell’s sign?
Upward movement of the eye on attempt to close the eye.
298
Why does hyperacusis occur in Bell’s palsy?
Involvement of the nerve supplying the stapedius muscle.
299
Recovery time for Bell’s palsy?
Most patients make a full recovery within 4 months.
300
Management of Bell’s palsy?
Prednisolone if patients present within 72 hours of onset.
Eye care: lubricating drops, tape eye shut when sleeping, wear sunglasses outdoors.
Straw for liquids and soft diet if chewing affected.
301
Cause of Bell’s palsy?
Thought to be related to inflammation and oedema of the facial nerve secondary to a viral infection or autoimmunity.
302
Anti-emetic example?
Ondansetron - 5-HT 3 receptor antagonist.
303
What is Paget's disease?
Chronic bone disorder characterised by focal areas of increased bone remodelling (increased osteoclast and osteoblast activity). This leads to osseous deformities, altered joint biomechanics, nerve compressions and pathological fractures.
304
Signs and symptoms of Paget's disease?
- long bone or back pain
- pathological fractures
- boney deformities (frontal bossing, prognathism, etc)
- hearing loss (skull involvement affecting CN VIII)
- facial pain (CN V)
305
Management of Paget's disease?
- bisphosphonates
- second line: calcitonin
- physiotherapy, analgesia, hearing aids
306
Where do primary brain tumours typically originate in adults?
Supratentorial (cerebrum).
307
Where do primary brain tumours typically originate in children?
Posterior fossa.
308
Types of glioma?
- astrocytoma
- oligodendroma
- ependymoma
309
Most common type of astrocytoma?
Glioblastoma
310
How aggressive are gliomas?
Graded from 1-4. 4 is most aggressive (e.g. glioblastoma).
311
What are some effects of meningiomas?
Usually benign, but mass effect can lead to raised ICP.
312
What are some effects of pituitary tumours?
- usually benign
- compression of optic chiasm (macroadenoma), leading to bitemporal hemianopia
- hypopituitarism
- excessive release of hormones (acromegaly, Cushing's disease, etc)
313
What is medulloblastoma?
Most common malignant brain tumour in children, arising from / near the cerebellum.
314
What is meningitis?
Inflammation of the meninges, usually due to a bacterial or viral infection.
315
What is meningococcal septicaemia?
Meningococcal bacterial infection present in the bloodstream. Causes disseminated intravascular coagulation and subcutaneous haemorrhage.
316
Is meningitis usually viral or bacterial?
Viral
317
Bacterial causes of meningitis?
- neisseria meningitidis
- streptococcus pneumoniae
- listeria monocytes (in elderly / immunocompromised)
318
Most common cause of meningitis in neonates?
Group B streptococcus
319
Viral causes of meningitis?
- enteroviruses
- herpes viruses
- mumps virus
- measles virus
320
Examples of herpes viruses?
- herpes simplex virus
- varicella zoster virus
- Epstein-Barr virus
321
Signs and symptoms of meningitis?
- fever
- headache
- neck stiffness
- nausea & vomiting
- photophobia
- altered consciousness
- seizures
- raised ICP (papilloedema and focal neurological signs)
- Kernig's and Brudzinski's signs
322
Which type of meningitis is most likely to cause raised ICP?
Bacterial
323
What is Kernig's sign?
Lower back pain on extension of knee when hip is flexed at 90 degrees. Due to stretch of the meninges.
324
What is Brudzinski's sign?
Patient lies on their back, flexion of the neck (lifting) causes reflex flexion of the hips.
325
Which type of meningitis is most likely to cause Kernig's / Brudzinski's signs?
Bacterial
326
Investigations for meningitis?
- blood culture
- viral stool and throat swab
- lumbar puncture and CSF analysis
- CT head BEFORE lumbar puncture if risk of cerebral herniation
327
CSF appearance viral vs bacterial?
bacterial - cloudy
| viral - clear
328
CSF protein viral vs bacterial?
bacterial - high
| viral - normal / mild elevation
329
CSF glucose viral vs bacterial?
bacterial - low
| viral - normal
330
CSF WBCs viral vs bacterial?
bacterial - high neutrophils
| viral - high lymphocytes
331
Empirical antibiotics for bacterial meningitis?
- cefotaxime / ceftriaxone
332
What additional empirical antibiotic should be used if there is a risk of listeria meningitis?
Ampicillin
333
Additional drug to treat bacterial meningitis, in addition to antibiotics?
Dexamethasone - to reduce neurological damage.
334
Post-exposure prophylaxis for contacts of bacterial meningitis?
Ciprofloxacin
335
Management of viral meningitis?
- supportive care
| - aciclovir may be used for herpes virus infection
336
Definition of encephalitis?
Inflammation of the brain parenchyma, usually caused by viruses.
337
Most common viral cause of encephalitis?
Herpes viruses are the most common group (herpes simplex virus, varicella zoster virus, cytomegalovirus, Epstein-Barr virus).
Herpes simplex virus type 1 is the most common cause.
338
Route of encephalitis infection?
- virus gains entry and replicates in local or regional tissue
- virus then reaches the CNS by haematogenous spread or retrograde axonal transport
339
Signs and symptoms of encephalitis?
- fever
- altered mental state
- focal neurological deficits
- seizures
- signs of causative viral infection (rash / cough / GI upset)
340
Gold standard investigation for encephalitis?
Lumbar puncture and CSF analysis (with viral PCR testing).
341
Management of encephalitis?
- empirical antiviral therapy (aciclovir)
| - supportive measures
342
Management of Wernicke's encephalopathy?
- IV thiamine
| - IV magnesium sulfate
343
Inheritance of Duchenne muscular dystrophy?
X-linked recessive
344
Pathophysiology of Duchenne muscular dystrophy?
Absence of dystrophin.
345
What is risperidone?
Anti-psychotic
346
What is conus medullaris syndrome?
Spinal cord injury at the level of the conus medullaris (L1) - results in UMN signs.
